Angiotensin II and VEGF are involved in angiogenesis induced by short-term exercise training

Amaral, Sandra Lia do; Papanek, Paula E.; Greene, Andrew S.

doi:10.1152/ajpheart.2001.281.3.h1163

Cited by 140 publications

(171 citation statements)

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“…Previous studies from our laboratory (2,3) demonstrated that the physiological inhibition of RAS with a high-salt diet or pharmacological inhibition with an angiotensin-converting enzyme inhibitor and ANG II type 1 receptor blocker significantly attenuates angiogenesis in skeletal muscle after electrical stimulation or exercise. The mechanisms responsible for these responses still need to be clarified.…”

Section: Discussionmentioning

confidence: 99%

Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake

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Amaral

Munzenmaier

et al. 2006

Physiological Genomics

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. Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake. Physiol Genomics 25: 325-335, 2006. First published February 7, 2006 doi:10.1152/physiolgenomics.00253.2005.-Angiogenesis, under normal conditions, is a tightly regulated balance between pro-and antiangiogenic factors. The goal of this study was to investigate the mechanisms involved in the control of the skeletal muscle angiogenic response induced by electrical stimulation during the suppression of plasma renin activity (PRA) with a high-salt diet. Rats fed 0.4% or 4% salt diets were exposed to electrical stimulation for 7 days. The tibialis anterior (TA) muscles from stimulated and unstimulated hindlimbs were removed and prepared for gene expression analysis, CD31-terminal deoxynucleotide transferase-mediated dUTP nick-end labeling (TUNEL) double-staining assay, and Bcl-2 and Bax protein expression by Western blot. Rats fed a low-salt diet showed a dramatic angiogenesis response in the stimulated limb compared with the unstimulated limb. This angiogenesis response was significantly attenuated when rats were placed on a high-salt diet. Microarray analysis showed that in the stimulated limb of rats fed a low-salt diet many genes related to angiogenesis were upregulated. In contrast, in rats fed a high-salt diet most of the genes upregulated in the stimulated limb function in apoptosis and cell cycle arrest. Endothelial cell apoptosis, as analyzed by CD31-TUNEL staining, increased by fourfold in the stimulated limb compared with the unstimulated limb. There was also a 48% decrease in the Bcl-2-to-Bax ratio in stimulated compared with unstimulated limbs of rats fed a high-salt diet, confirming severe apoptosis. This study suggests that the increase in endothelial cell apoptosis in TA muscle might contribute to the attenuation of angiogenesis response observed in rats fed a high-salt diet.Bax; Bcl-2; gene expression THE GROWTH OF NEW BLOOD VESSELS plays a critical role in normal physiological processes but is also central to the progression of many diseases. Angiogenesis is involved in several disorders such as cancer, diabetic retinopathy, macular degeneration, and endometriosis (15). In an attempt to control pathological angiogenesis, a growing interest in better understanding prosurvival and prodeath signals has emerged (7,8,26,34). Each endothelial cell within a vessel wall is exposed to a combination of prosurvival and prodeath signals. The sum of these signals determines whether the cell remains viable or undergoes apoptosis (10).Our laboratory has demonstrated that physiological, pharmacological, or genetic manipulation of the renin-angiotensin system (RAS) has an important impact on both the basal number of microcirculatory blood vessels and the ability of tissues to undergo angiogenesis induced by exercise (3) or electrical stimulation (2). In previous studies (4), we demonstrated that transfer of a region of chromosome 13 containing the renin gene from Dahl R into Dahl S rats restores both p...

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Section: Discussionmentioning

confidence: 99%

Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake

Resende

Amaral

Munzenmaier

et al. 2006

Physiological Genomics

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“…First, increases in IGF-1 and VEGF occur peripherally in response to activity to stimulate tissue and vascular system growth and repair, which improves oxygen delivery to muscles and increases aerobic performance [49,50]. For example, VEGF signalling regulates muscle capillary density, which is a major determinant of maximal aerobic capacity across mammals [51,52]. Second, BDNF and IGF-1 facilitate lipid oxidation in muscles [53] and glucose metabolism [1], which are essential for energy regulation during submaximal activity [54].…”

Section: (A) Neurotrophins and Growth Factorsmentioning

confidence: 99%

“…The relationship between VO 2,max and brain size across mammals is likely to be related to differences in VEGF expression in more athletic taxa [6], because VO 2,max is positively correlated with the volume of muscle capillary networks across mammals, driven by the need to deliver oxygen during APA [52]. Because skeletal muscle capillarity is regulated by VEGF [51,69], the increased volume of the capillary network found in mammals with high aerobic capacities may be due to evolutionarily altered VEGF signalling.…”

Section: Evolutionary Links Between Aerobic Physical Activity and Neumentioning

confidence: 99%

Linking brains and brawn: exercise and the evolution of human neurobiology

2013

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The hunting and gathering lifestyle adopted by human ancestors around 2 Ma required a large increase in aerobic activity. High levels of physical activity altered the shape of the human body, enabling access to new food resources (e.g. animal protein) in a changing environment. Recent experimental work provides strong evidence that both acute bouts of exercise and long-term exercise training increase the size of brain components and improve cognitive performance in humans and other taxa. However, to date, researchers have not explored the possibility that the increases in aerobic capacity and physical activity that occurred during human evolution directly influenced the human brain. Here, we hypothesize that proximate mechanisms linking physical activity and neurobiology in living species may help to explain changes in brain size and cognitive function during human evolution. We review evidence that selection acting on endurance increased baseline neurotrophin and growth factor signalling (compounds responsible for both brain growth and for metabolic regulation during exercise) in some mammals, which in turn led to increased overall brain growth and development. This hypothesis suggests that a significant portion of human neurobiology evolved due to selection acting on features unrelated to cognitive performance.

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“…This was likely to be due to the different time course of gene activation versus protein expression. The mRNAs for these molecules tend to increase early in the training and are transient [27] ; by the time we assayed the tissues (after four weeks' training), the mRNA levels had declined to protect against the negative effects of ACE overexpression [28][29][30][31] . Thus, these data indicated that the LHTL training protocol markedly decreased ACE gene expression which some studies have suggested that down-regulation of ACE gene expression was beneficial for long-term exercise training [15] .…”

Section: Wwwchinapharcom Shi W Et Almentioning

confidence: 92%

“…(E and F) shows that the endocardium is thinner in the LLS heart compared to the LHTL heart. [27] . In addition, the over-expression of ACE can cause adaptive hypertrophy of the cardiac muscle, resulting in reduced cardiac contractility and various pathologies that can be reversed through the administration of ACE inhibitors [32] .…”

Section: Wwwchinapharcom Shi W Et Almentioning

confidence: 99%

Living high training low induces physiological cardiac hypertrophy accompanied by down-regulation and redistribution of the renin-angiotensin system

et al. 2013

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Aim: Living high training low" (LHTL) is an exercise-training protocol that refers living in hypoxia stress and training at normal level of O 2 . In this study, we investigated whether LHTL caused physiological heart hypertrophy accompanied by changes of biomarkers in reninangiotensin system in rats. Methods: Adult male SD rats were randomly assigned into 4 groups, and trained on living low-sedentary (LLS, control), living lowtraining low (LLTL), living high-sedentary (LHS) and living high-training low (LHTL) protocols, respectively, for 4 weeks. Hematological parameters, hemodynamic measurement, heart hypertrophy and plasma angiotensin II (Ang II) level of the rats were measured. The gene and protein expression of angiotensin-converting enzyme (ACE), angiotensinogen (AGT) and angiotensin II receptor I (AT 1 ) in heart tissue was assessed using RT-PCR and immunohistochemistry, respectively. Results: LLTL, LHS and LHTL significantly improved cardiac function, increased hemoglobin concentration and RBC. At the molecular level, LLTL, LHS and LHTL significantly decreased the expression of ACE, AGT and AT 1 genes, but increased the expression of ACE and AT 1 proteins in heart tissue. Moreover, ACE and AT 1 protein expression was significantly increased in the endocardium, but unchanged in the epicardium. Conclusion: LHTL training protocol suppresses ACE, AGT and AT1 gene expression in heart tissue, but increases ACE and AT 1 protein expression specifically in the endocardium, suggesting that the physiological heart hypertrophy induced by LHTL is regulated by regionspecific expression of renin-angiotensin system components.

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Angiotensin II and VEGF are involved in angiogenesis induced by short-term exercise training

Cited by 140 publications

References 39 publications

Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake

Role of endothelial cell apoptosis in regulation of skeletal muscle angiogenesis during high and low salt intake

Linking brains and brawn: exercise and the evolution of human neurobiology

Living high training low induces physiological cardiac hypertrophy accompanied by down-regulation and redistribution of the renin-angiotensin system

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